PHB3 Regulates Lateral Root Primordia Formation via NO-mediated Degradation of AUX/IAAs

Abstract

We previously showed that PHB3 regulates auxin-stimulated lateral root (LR) formation; however, the underlying molecular mechanism is unknown. Here, we demonstrate that PHB3 regulates LR development mainly through influencing lateral root primordia (LRP) initiation via affecting nitric oxide (NO) accumulation. The reduced LRP in phb3 was largely rescued by exogenous NO donor SNAP treatment. The decreased NO accumulation in phb3 caused a lower expression of GATA23 and LBD16 through inhibiting the degradation of IAA14/28. Overexpression of either GATA23 or LBD16 in phb3 mutant background recovered the reduced LRP number phenotype. These results indicate that PHB3 regulates LRP initiation via NO-mediated auxin signaling through regulating the degradation of IAA14/28. HighlightPHB3 regulates IAA28 and IAA14 degradation by controlling NO accumulation, and thereby regulating LR founder cell identification and the transition to asymmetric division.